T allele presence eases effect of air pollution on RA-ILD risk

People exposed to air pollution for too long are at greater risk of developing rheumatoid arthritis (RA)-associated interstitial lung disease (ILD), with the effect potentially modified according to MUC5B rs35705950 genotype, reveals a study.

A total of 594 patients with RA (mean age 58 years, 71 percent women, 44 percent current or former smokers) who had undergone high-resolution CT (HRCT) of the chest were included in the analysis.

The researchers obtained MUC5B status when available and estimated exposure levels to NO₂, PM₁₀, and PM_2.5 based on residential postal code using a dispersion model. They examined the influence of air pollution on ILD occurrence using logistic regression and explored the interaction between air pollution and MUC5B.

Of the patients, 227 (38 percent) developed ILD, and 292 were genotyped for MUC5B rs35705950. After adjusting for age, sex, smoking status, and HRCT year, an association was found between increased long-term exposure to NO₂ (odds ratio [OR], 1.04, 95 percent confidence interval [CI], 1.01–1.06), PM_2.5 (OR, 1.11, 95 percent CI, 1.10–1.24), and PM₁₀ (OR, 1.15, 95 percent CI, 1.05–1.26) and ILD.

Notably, a negative interaction was observed between PM₁₀/PM_2.5 exposure and the T allele, suggesting that the presence of the minor T allele weakened the influence of air pollution on ILD risk.

“RA-ILD and idiopathic pulmonary fibrosis share common risk factors, including the MUC5B promoter variant (rs35705950),” the researchers said.